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Treatment of Facial
Paralysis
Omid B. Mehdizadeh, MDa, Jacqueline Diels, OTb,
William Matthew White, MDc,*
KEYWORDS
Synkinesis Facial paralysis Botulinum toxin Asymmetry
KEY POINTS
Combination treatment with neuromuscular retraining (NMR) exercises is essential for a better long-
term outcome.
A sequence of first evaluation and treatment with NMR is recommended. When resistant muscle
groups are identified, treatment should be started with chemodenervation.
Botulinum toxin can be injected in the affected synkinetic hemiface to relax hyperactive muscles
and the normal hemiface for balance to restore facial symmetry.
Challenging areas for treatment of synkinesis include the midface and lip depressor complex and
should be addressed carefully.
a
NYU Langone Medical Center, 550 First Avenue - NBV 5E5, New York, NY 10016, USA; b Facial Nerve Clinic,
UW Hospitals and Clinics, 600 Highland Avenue, Madison, WI 53792, USA; c NYU Ambulatory Care Center, 240
E 38th Street, 14th Floor, New York, NY 10016, USA
* Corresponding author.
E-mail address: William.white@nyumc.org
Pattern of injection into muscle groups, units with “misdirection of the facial nerve” after Bell’s
administered, and frequency of treatment is not Palsy causing ocular spasm with smiling.20 Since
standardized. Amounts administered have varied then, the literature has been populated by
from fractions of a unit per site9 to hundreds in numerous studies augmenting the role of botulinum
total,5,10,11 with increasing risk of adverse events toxin A in postparalytic facial synkine-
including oral incompetence, ptosis, diplopia, sia5,9–12,15,21–29 evolving to hints of long-term
exposure keratopathy, malaise, and worsened improvement when used with concurrent neuro-
cosmesis10,12 with larger doses. These events muscular training including half and whole face
are reversible, however, because the effects of mirror feedback6,7 and neuromuscular retraining
the toxin diminish. (NMR) therapy.26 The application of other tradi-
Botulinum toxin continues to expand from its tional therapies in conjunction with botulinum toxin
first description in strabismus by Scott13 in 1980 has yet to be elucidated.
to its eventual approval by the US Food and Causes of postparalytic facial synkinesia are
Drug Administration for strabismus and blepharo- vast and varied, providing a universal platform for
spasm in 1989. Additional benefits were recog- this minimally invasive therapy. Central iatrogenic
nized for aesthetic purposes by Carruthers and tumor resections in the setting of vestibular and
Carruthers14 in their description of reduction in facial schwannomas,27 middle ear surgery,24 as
glabellar frown lines in 1992. well as peripheral parotid malignancies have
Those who endure the sequela of postparalytic been described.27 Bells palsy and Ramsey Hunt
synkinesis or abnormal involuntary facial move- syndrome have also been implicated,9,19,27 in
ments have been shown to have diminished qual- addition to traumatic skull base injury.9
ity of life, social interactions, peripheral visual The neurophysiology of these involuntary move-
impairment, and a worsened self-impression of ments has yet to be fully understood. Aberrant
personal appearance. In many instances, botuli- peripheral facial nerve regeneration is most
num toxin therapy has been shown to decrease commonly attributed.30–32 However, studies in
the severity of these personal morbidities and the generation of synkinesis have demonstrated
improve quality of life15 with validated methods predictable patterns of regeneration thought to
of subjective assessment including the Facial be owing to increased excitability within the facial
Clinimetric Evaluation score,16 Sunnybrook Facial nucleus itself.33
Grading System,17 and Synkinesis Assessment This article reviews the current literature sup-
Questionnaire18 currently in use. porting the use of botulinum toxin in producing
Characterized by involuntary movement in the symmetric facial features and reducing unwanted,
setting of volitional facial expressions, multiple involuntary movements. Methods, protocols, and
patterns have been described after facial nerve adverse events are discussed. Additionally, the
injury including ocular, oral, and cervical synkine- authors suggest that using botulinum toxin A ther-
sias, dyskinesias, and hyperkesias. Typically, a apy in postparalytic facial synkinesis can provide
patient might experience spasm of the eye with long-term results when used in conjunction with
smiling or sometimes violent movements of the other treatment modalities.
corner of the mouth with eye closure. Manifesta-
tions of various forms require personalized injec- EVALUATION
tion patterns to achieve optimal outcomes and
aesthetics while minimizing side effects.5 The toxin Before beginning therapy, a patient should
is typically administered to certain muscle groups undergo a thorough evaluation of their history of
that provide certain function (ie, eye closure or facial paralysis and a complete evaluation of their
lip elevation) such as injection into the orbicularis facial movements. Standardized photography and
oculi, corrugators, and frontalis muscles for upper video recording should be performed to clearly
synkinesias and zygomaticus, levator muscle document treatment efficacy. The 9 standard
of upper lip, orbicularis oris, depressor labii, views include face at rest, brow elevation, com-
depressor oris, and platysma muscles for lower plete eye closure, nose wrinkling, grin, full smile,
division defects.7,19 Functionally, botulinum toxin pucker, whistle, and lower lip depression.
chemically dennervates the neuromuscular junc- It is important during the evaluation to identify
tion by permanently blocking presynaptic acetyl- the “triggers” for eliciting the synkinesis. This
choline release at the synaptic junction. most commonly is forceful eye closure or a puck-
Mention of botulinum toxin A as an alternate ering movement of the lips. Critical to the evalua-
treatment of ocular synkinesia was first introduced tion, the patient should be questioned their main
by Putternam20 in 1990. In his description of a sin- concerns are and what areas of the face and
gle case report, he discusses a 28-year-old woman neck are the most troubling. Patients typically
Treatment of Facial Synkinesis 13
remark about the discomfort of spasms around the is no precedent for identifying and understanding
eye or neck. Ideally, these areas should be ad- it. When muscles contract out of sequence, the
dressed first and foremost. It is recommended to facial skin is displaced in an unusual direction,
wait at least 6 months after the onset of facial pa- creating a distorted expression. What seems to
ralysis to allow recovery. Any intervention before be lack of movement caused by weakness
that time can potentially make the synkinesis may in fact be abnormal hyperactivity of an
worse. opposing muscle restricting range of motion
Ideally, the patient should have an initial treat- and excursion.
ment by a physical or occupational therapist who Comprehensive retraining incorporates signifi-
has specific training in facial NMR. It is helpful for cant education regarding facial anatomy and mus-
the physician to evaluate the patient before begin- cle actions. This is key to comprehending the true
ning therapy, which can help to determine the nature of the disability, that is, the difference be-
progress of treatment. A team approach can be tween a deficiency of muscle activity resulting in
very helpful to the patient. no movement (flaccidity) and aberrant muscle ac-
tivity (synkinesis) resulting in wrong movement. In
THERAPEUTIC OPTIONS
Neuromuscular Retraining
Facial NMR is a specific subset of occupational
and physical therapy developed for improving
motor learning and functional outcomes in patients
with facial paralysis, paresis and/or synkinesis af-
ter facial nerve injury. Facial NMR techniques are
based on characteristics unique to the facial nerve
and muscles it innervates (eg, lack of muscle
spindles and presence of emotional, as well as
volitional, neural inputs).34 Facial NMR should not
be confused with the more common, nonspecific
therapies that promote gross motor, maximum
effort exercises and electrical stimulation, both of
which are contraindicated in facial paralysis.35
Rather, NMR focuses on providing sensory infor-
mation to enhance neural adaptation and learning
via the practice of minimal, precisely coordinated
movement patterns in conjunction with modalities
such as surface electromyographic, propriocep-
tive, and mirror feedback. This comprehensive
clinical program was first described by Balliet
and colleagues36 in 1982, who reported improved
function in patients more than 2 years after facial
nerve injury. Acquisition of new motor behaviors
was attributed to brain plasticity, the capacity of
Fig. 1. Muscles of facial expression (arrows depict
the central nervous system to modify its organiza- normal direction of contraction). Muscles: BUC, bucci-
tion, resulting in lasting functional change.36 nators; COM, compressor naris; COR, corrugator;
From a nonoperative rehabilitation perspective, DAO, depressor anguli oris; DIN, dilator naris; DLI,
facial muscles play a different role than other mus- depressor labii inferioris; FRO, frontalis; LAO, levator
cles in the body. Simply stated, their purpose is to anguli oris; LLA, levator labii alaeque nasi; LLS, levator
move the facial skin in various directions, produc- labii superioris; MEN, mentalis; OCI, orbicularis oculi
ing a wide variety of expressions used primarily for inferioris; OCS, orbicularis oculi superioris; OOI, orbi-
nonverbal communication, eye closure, and oral cularis oris inferioris; OOS, orbicularis oris superioris;
PLA, platysma; PRO, procerus; RIS, risorius; ZYJ, zygo-
motor functions. The subtleties of human expres-
maticus major; ZYN, zygomaticus minor. Facial nerve
sion require a delicate balance of activity among
branches: B, buccal; C, cervical; M, mandibular; T, tem-
multiple facial muscles. The presence of synkine- poral; Z, zygomaticus. (Adapted from Balliet R. Facial
sis destroys the normal balance. paralysis and other neuromuscular dysfunctions of the
Synkinesis is the most common condition peripheral nervous system. In: Payton OD. Manual of
treated by the facial NMR therapist. Because it physical therapy. New York: Churchill Livingstone;
does not occur in other areas of the body, there 1989. p. 179; with permission.)
14 Mehdizadeh et al
cases of synkinesis, the common practice of pre- keeping with the patient’s stated goals, without
scribing maximum effort movements (in an erro- causing additional morbidity. Targeting the most
neous attempt to strengthen muscles) intensifies appropriate injections sites for the best outcome
the abnormal response, reinforcing the synkinesis. is challenging owing to the complex interactions
Appropriate intervention focuses on accurately of the facial muscles. Knowledge of anatomy is
coordinating viable, albeit synkinetic, muscles not enough. It is also essential to know the working
rather than stimulating flaccid ones. With skilled action of each muscle, both in isolation and in
training it is possible to improve movement pat- conjunction with the actions of others.
terns and expression even many years after synki- The most common injection sites include the or-
nesis develops.35,36 bicularis oculi, corrugator, platysma, and mentalis
When used in conjunction with facial NMR, bot- muscles (Fig. 1). Recently, minimal dose injections
ulinum toxin provides a “window of opportunity” to the synkinetic buccinator have proven to be of
during which the patient can learn and practice benefit in improving outcomes.37 The midfacial
isolated, coordinated movement patterns without muscles are rarely injected to avoid creating weak-
the cocontraction and restriction caused by synki- ness in key areas targeted during the NMR pro-
nesis. It is preferable to complete 6 months of re- cess, such as smile. For greatest accuracy in
training before injecting botulinum toxin to enable targeting injection sites, the patient is asked to
the patient to learn the synkinesis inhibition tech- demonstrate the expressions that elicit the synki-
niques. The presence of botulinum toxin before netic response. Forceful eye closure, smile,
retraining does not afford this same learning pucker and snarl will most commonly produce
opportunity. the response. Each movement may elicit a unique
The retraining therapist, as part of the multidisci- synkinetic pattern, so all should be tested. It is
plinary team, is instrumental in precisely identi- important to note that even a region demonstrating
fying the synkinetic muscles most restricting little to no volitional activity (e.g. forehead) can
normal function. These, when injected, should demonstrate significant aberrant activity in a syn-
allow for greater ease and range of motion in kinetic pattern, so should be evaluated in that
Fig. 2. Treatment of Synkinesis in the Peri-Ocular Area. (A) Patient with visible synkinesis in the right orbicularis
oculi muscle. Botulinum toxin was injected in the right periorbital area displayed in the figure (doses are in Units,
Black 5 1cc dilution). (B) One month after botulinum treatment showing improved eye opening.
Treatment of Facial Synkinesis 15
context. (In such a case, no brow movement is on the nasolabial fold can result in the lack of func-
observed when the patient attempts to raise it voli- tion of the smiling muscles and cause great distress
tionally, however, significant elevation may occur to patients for 3 to 4 months until the effect of the
during smile or pucker). drug wears off. Patients most often state that they
would prefer the increased muscle tension, rather
Neuromodulator Injection than looking “paralyzed,” with complete muscle
inactivity. For this reason, NMR is a critical aspect
When the botulinum toxin vials arrive, they are to address tension in the cheek. Neuromuscular re-
frozen and need to be reconstituted with normal taining can often be a safer, much more effective
saline. The authors use 2 main preparations of intervention than botulinum toxin injection in
botulinum toxin, a 1 mL dilution (10 units per relieving the painful spasm in the cheek.
each 0.1 mL) and a 2 mL dilution (5 units per Occasionally, one can elicit spasm in the area of
each 0.1 mL). The 1 mL dilution provides a solution the zygomaticus minor muscle, located in the na-
that allows a more targeted approach to muscle solabial fold just about one-third of the distance
relaxation, particularly in the medial midface zygo- from the nasal ala to the lateral commissure
matic complex and the periocular areas. The 2 mL (Fig. 3). A precise injection of botulinum toxin of
dilution allows for much greater diffusion of the 0.5 to 1 unit, with a concentrated 1 mL dilution of
toxin, and can be advantageous in larger muscles, product to minimize diffusion, can be very effec-
such as the platysma. tive. Injecting over the malar eminence high and
After the injection, patients should avoid any lateral in the cheek is not recommended because
physical activity or facial exercises for 2 days to this leads frequently to complete weakness of
prevent diffusion of the product to unwanted areas. the zygomatic muscle complex.
Botulinum toxin starts to take effect in 3 to 5 days
and the peak effect is routinely seen at 2 weeks. Perioral The most frequent complaint that we
For that reason, we usually recommend that pa- hear from patients is the inability to achieve what
tients follow up 1 month after treatment to assess
efficacy of the treatment. At that point, any addi-
tional areas that did not respond as well as desired
can be treated with additional botulinum toxin. It is
highly recommended to begin conservatively with
the patient’s first treatment, and then titrate the bot-
ulinum toxin dose upward as needed.
Periocular
The forehead and periocular area contains the
muscles that both elevate and depress the brow
complex. The frontalis muscle is the main elevator
of the eyebrows, and the corrugator supercilli and
orbicularis oculi are the main depressors of the
eyebrows. Spasm of the frontalis and corrugator
supercilli muscles are frequent causes of tension
headache pain in synkinesis patients, and can
often be elicited with a careful history and exami-
nation. Additionally, one of the most frequent com-
plaints of patients with synkinesis is the tight
spasm that can occur in the orbicularis oculi mus-
cle. This causes a narrowing of the visual field in
the effected eye, painful spasm of the muscle,
and exaggeration of the crow’s feet area (Fig. 2).
Midface One of the most challenging areas to inject
is the cheek and midface area, because spasm of
Fig. 3. Spasm of the Zygomaticus Minor. (A) In the
the zygomatic muscles leads to pain and discom-
right hemi-face, forceful eye closure triggers spasm
fort in the cheek. Unfortunately, this is the area of the right Zygomaticus Minor muscle. Botulinum
that is most frequently cited by patients as being toxin was injected in the area just anterior to the right
the most bothersome in terms of pain and discom- nasolabial fold displayed in the figure (doses are in
fort. The lower face is also the most challenging Units, Black 5 1cc dilution). (B) One month following
area to inject. Overinjection of the muscles acting treatment, there is reduced spasm in the right cheek.
16 Mehdizadeh et al
they know as a normal smile. This can be caused limiting exposure of the upper teeth and upward
by a variety of factors including the downward pull movement of the smile.
of lip depressor muscles that prevent lateral up-
ward excursion of the lateral commissure. Tar- Neck
geted treatment of the platysma, depressor labi Tense spasm of the platysma muscle on the
inferioris, and depressore anguli oris is quite help- affected side is a freqent complaint among synki-
ful. Symmetry of the lower lip, particularly during nesis patients. The medial fibers contribute to the
smiling is very important, and injection of the depressor function of the lateral oral commis-
contralateral lip depressor muscles can often be sure, and can act as a pulley that pulls the corner
helpful. of the mouth in a downward direction. This
A typically overlooked muscle that can limit downward traction of the platysma muscle inter-
lateral excursion of the smile is the buccinator mus- feres with smiling as it acts against the zygomatic
cle (Fig. 4). The Buccinator muscle is an accessory muscles to allow upward and lateral excursion of
muscle for mastication, but is controlled by the the oral commissure. As a result, after treating
buccal branch of the facial nerve. The muscle’s the platysma muscle with botulinum toxin, pa-
main action is to pull the lateral commissure of tients usually report improvement in their ability
the mouth posteriorly and to tense and flatten the to smile on the affected side. Typical injection
mucosal surface of the cheek against the teeth. In doses in the platysma muscle are 15 to 20 U of
doing so, the angle of the mouth is pulled closed. botulinum toxin (Fig. 6). We typically use 2 cc di-
Spasm of the buccinator muscle pulls the corner lutions to facilitate even spread of the drug within
of the mouth posteriorly on the synkinetic side, the muscle.
Fig. 4. Synkinesis of the buccinator muscle. (A) Simulation of buccinator spasm and the effect on the oral commis-
sure. This patient had left facial synkinesis, with image (B) displaying the normal, unaffected side. Compare to (C),
showing synkinetic muscular activity upon forcefull eye closure. Note the spasm and bulge of the buccinator
muscle.
Treatment of Facial Synkinesis 17
neck crease. A history of relief of pain and discom- RT001 has not been studied in synkinesis, but it
fort from synkinesis with botulinum toxin injections seems ideally positioned to address synkinetic
is usually a good predictor of a successful facial muscles that located more superficially in
mymectomy. the facial soft tissues, such as the orbicularis oculi
and orbicularis oris. A superficial location and
FUTURE DIRECTIONS nearby proximity to the skin would theoretically
minimize the distance for absorption and have a
One of the downsides of neuromodulator treat- greater chance of success.
ment of synkinesis is that injections must be The second product, RT002, is a new injectable
repeated every 3 months. Second, injections are formulation of the botulinum toxin that was de-
performed with very small needles and are quite signed to offer a more target delivery of the botu-
well-tolerated; however, there is some discomfort linum toxin and reduce the spread of toxin
associated with the treatment. One new pharma- beyond the site of injection.40 Again, RT002 has
ceutical company, Revance Therapeutics, has not been studied in synkinesis patients, but seems
developed new neuromodulators to address ideally suited to precisely target a facial muscle in
some of these issues. spasm, while sparing a nearby, uninvolved mus-
The first product, RT001, is a topical gel formu- cle. RT002 has currently completed phase II clin-
lation of the botulinum toxin type 1.39 The drug is ical trials for cosmetic glabellar frown lines and
applied to the skin at precise locations, and after functional cervical dystonia. One encouraging
sufficient time is absorbed and delivers its effect. finding from the clinical studies was that RT002
The company is targeting a cosmetic indication achieved a median duration effect of 7 months.
for crow’s feet lines. The drug has shown prom- The longer duration of effect might reduce the
ising results in more than 17 clinical studies and number of visits that synkinesis patients typically
is currently in phase III clinical trials. Topical need.
Fig. 6. Injection of contralateral lip depressors improves the smile. (A) Patient with visible synkinesis in the left
hemiface, botulinum toxin was injected into the affected left face, and the contralateral right lip depressors
(doses are in Units, Black 5 1cc dilution; Yellow 5 2cc dilution). (B) One month after botulinum treatment
showing a balanced smile.
Treatment of Facial Synkinesis 19
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